Decades of research have highlighted the damaging effects of prenatal exposure to common environmental toxicants (i.e., tobacco smoke, lead, and mercury) on later health outcomes. Fetuses and infants are particularly sensitive to such exposure, both because early disruptions in development can have long-lasting effects, but also because many neurotoxicants are readily transferred across the placenta and the fetal blood brain barrier. Not surprisingly, then, children born in areas with high levels of pollutants (e.g., poor urban neighborhoods) suffer from notably higher rates of a number of adverse health outcomes, including child behavior problems (BP) such as aggression, antisocial behavior, and hyperactivity. Although few would now contest the behavioral sequelae of prenatal pollutant exposure, the mechanism(s) driving these effects are as yet unclear. Studies of alterations in resting-state functional connectivity (RSFC) during the fetal period represent a particularly promising avenue for such research, since RSFC has been shown to initially develop in utero and has been associated with both youth BP and toxicant exposure during childhood. The goal of this R21 is to examine associations between prenatal exposure to three common toxicants (tobacco smoke, lead, and mercury) and fetal RSFC at 35-weeks gestation, and the longitudinal consequences of these associations for child BP. We will first establish prenatal exposure to lead, mercury, and/or cotinine as predictor(s) of RSFC in the developing fetal brain. We will next evaluate fetal RSFC as a predictor of BP at age 3. We will then examine whether fetal RSFC mediates associations between child BP and prenatal toxicant exposure. We will thus be able to meaningfully evaluate whether and how prenatal toxicant exposures affect functional neurocircuitry of the developing fetal brain, and the long-term behavioral consequences of those associations. Such work would constitute a substantial advance in our understanding of not only the long-term effects of prenatal toxicant exposure, but also the origins of child BP.